New HIV drug class forms deal focus
million) service agreement with Schering-Plough Research Institute,
to use ViroLogic's novel HIV resistance testing technology to
support Schering-Plough's drug R&D into a new class of HIV
drug.
Schering-Plough plans to use ViroLogic's assays for the clinical development of its CCR5 receptor antagonist, vicriviroc, a potential new drug for HIV infection. CCR5 receptor antagonists are a type of HIV Entry Inhibitor, a class of drugs that is a promising new treatment option for HIV-infected individuals.
A new class of HIV drugs is considered a major step towards effective treatment in halting the progress of the disease. Considering that some current antiretrovirals drugs were launched between the years 1990 to 2000, new treatments that have a slower pill burden, higher potency and fewer incidences of adverse side effects are urgently needed.
Pharmaceutical companies that have drug candidates with efficacy against resistant strains or novel having mechanisms of action now dominate the pipeline.
US-based Samaritan Pharmaceuticals is currently in phase II/III of SP-01A, its new drug candidate that blocks the AIDS virus before it ever enters the human cell. SP-01A cripples HIV's ability to enter cells by blocking the proteins on Human T Cells that would, otherwise, facilitate HIV's entry into those cells
Other pharmaceutical companies that are involved in the development of HIV Entry Inhibitor drugs include Pfizer and Glaxosmithkline.
The Phase III program for vicriviroc is scheduled to commence in 2005 and will use ViroLogic's PhenoSense HIV Co-receptor Tropism assay to identify and monitor patients during the trials.
"ViroLogic pioneered the use of testing to help guide better treatment of patients, and we believe our tests have enabled breakthroughs in the way clinical trials are designed." said Bill Young, ViroLogic's chairman and chief executive officer.
As recommended by the US FDA Antiviral Drugs Advisory Committee, biopharmaceutical companies are using HIV resistance testing technology to enhance next-generation HIV drug development.
Resistance typically occurs as a result of mutations in HIV's genetic structure (RNA). Mutations of RNA lead to alterations in certain proteins, most commonly enzymes that regulate the production of infectious virus. Mutations are especially common in HIV, as this virus reproduces at an extraordinary rate and does not contain the proteins needed to correct mistakes made during copying of the genetic material.
HIV relies on many enzymes, such as reverse transcriptase, integrase, and protease to replicate inside a human cell. If a mutation of a single site in the reverse transcriptase gene occurs, the change will remain with the virus as long as it replicates or until another copying error alters its form yet again. Some mutations cause the virus to become so weak that it cannot replicate effectively; other mutations may cause the virus to become even more virulent.
Antiretroviral drugs, disrupt the HIV enzyme's ability for genetic copying, or making virus that can infect other cells. In a person who takes antiretroviral drugs, most of the HIV are killed or prevented from multiplying further.
Some strains of HIV are naturally resistant to the presence of such drugs. That is why treatment with monotherapy (a single antiretroviral drug) is destined to fail.
Current figures estimate that up to 270,000 US patients are resistant to at least one class of HIV drug. Around 50,000 have developed resistance to all three currently available drug classes.
In addition, up to 20 per cent of new infections now involve the transmission of resistant virus, meaning new classes of HIV drugs (especially against novel targets) will provide the only hope of treatment for an increasing number of patients.
